The kidney which is vital for the restoration of plasma composition following perinatal asphyxia, is itself adversely affected by hypoxemic insults. This research is designed to examine the role and the interaction between some vasoactive mediators in the regulation of fetal renal function and its adaption to extrauterine life. We also propose to investigate the effects of acute perinatal asphyxia on these control processes and to relate them to hormone levels in the fetus. Finally, we plan to examine the possibility that profound fetal asphyxia results in overstimulation of the pituitary, adreno-sympathetic and renin-angiotensin systems. We propose to study the renal function and regional circulation in relation to plasma catecholamines, vasopressin and renin-angiotensin in the sheep under the following conditions: (a) normal gestation, labor and the immediate neonatal period; (b) intrauterine asphyxia with or without vasoactive antagonists, and (c) exogenous administration of vasoactive mediators to the fetus and newborn. Our current work on the fetal lamb has shown that excessive excretion of fluid and electrolytes with or without changes in glomerular filtration occurs during experimental intrauterine asphyxia. These studies suggest that the maintenance of homeostasis by the kidney is modulated by the interaction of various vasoactive mediators released during asphyxia and raise the possibility of prolonged biological action by these mediators if the asphyxial stimulus is severe.